anti-Hairless (HR) Antikörper

May act as a transcription factor that could act on to regulate one of the phases of hair growth.. Zusätzlich bieten wir Ihnen Hairless Proteine (5) und viele weitere Produktgruppen zu diesem Protein an.

HR Antikörper nach Reaktivität, Anwendung, Klonalität and Konjugat

Weitere Produktkategorien zu Hairless Antikörper

Weitere Antikörper gegen Hairless Interaktionspartner

Human Hairless (HR) Interaktionspartner

mammalian Hr is a phosphoprotein which can exert cross-talk with the p53 (zeige TP53 Antikörper) pathway with important implications for the regulation of cell proliferation and differentiation in tissues such as skin and brain where Hr is highly expressed.

We have identified two recurrent missense mutations in U2HR c.1A>T (p. Met1?) and c.104A>G (p.*35Wext1263*) in two Chinese Han families with Marie Unna Hereditary Hypotrichosis.

study reports two cases of Marie Unna hereditary hypotrichosis; a novel nonsense mutation of U2HR was identified in the second case, but no causative mutation in U2HR or EPS8L3 (zeige EPS8L3 Antikörper) was found in the first case

we have identified a mutation, c.74C>T, in a Chinese family with MUHH, which has been previously described in a family from Hungary. Our findings therefore indicate the prevalence of this mutation in diverse populations.

Findings indicate that hairless (HR) is a H3K9 demethylase (zeige MBD2 Antikörper) that regulates epidermal homeostasis via direct control of its target genes.

deletion mutants of hairless indicate that the JmjC domain contributes to the co-repressor activity

Mutations in the gene HR coding for the hairless protein are associated with an autosomal recessive form of alopecia universalis

Marie Unna hereditary hypotrichosis is caused by a novel mutation (U2HR) in the human hairless transcript.

study reports a family with Marie Unna hereditary hypotrichosis (MUHH) from Turkey; identified the mutation c.2T > C (M1T) in all affected family members; concluded that there may be considerable clinical variations in MUHH

Mouse (Murine) Hairless (HR) Interaktionspartner

This study examinedthe uncommon phenotype and using microarray analyses and functional studies, we found that beta-catenin was mediated by Hr. Progenitor keratinocytes from the bulge region differentiate into both epidermis and sebaceous glands, and fail to adopt the hair keratinocytes fate in the mutant scalp, due to the decreased Wnt/beta-catenin signaling in the absence of the hairless protein.

Hairless (HR) Antigen-Profil

Protein Überblick

This gene encodes a protein that is involved in hair growth. This protein functions as a transcriptional corepressor of multiple nuclear receptors, including thyroid hormone receptor, the retinoic acid receptor-related orphan receptors and the vitamin D receptors, and it interacts with histone deacetylases. The translation of this protein is modulated by multiple regulatory ORFs that exist upstream of the primary ORF. Mutations in one of these upstream ORFs, U2HR, cause Marie Unna hereditary hypotrichosis (MUHH), an autosomal dominant form of genetic hair loss. Mutations in this gene also cause autosomal recessive congenital alopecia and atrichia with papular lesions, other diseases resulting in hair loss. Two transcript variants encoding different isoforms have been found for this gene.